Plasma metabolomics supports the use of long-duration cardiac arrest rodent model to study human disease by demonstrating similar metabolic alterations

Muhammad Shoaib, Rishabh C. Choudhary, Jaewoo Choi, Nancy Kim, Kei Hayashida, Tsukasa Yagi, Tai Yin, Mitsuaki Nishikimi, Jan F. Stevens, Lance B. Becker, Junhwan Kim

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

Cardiac arrest (CA) is a leading cause of death and there is a necessity for animal models that accurately represent human injury severity. We evaluated a rat model of severe CA injury by comparing plasma metabolic alterations to human patients. Plasma was obtained from adult human control and CA patients post-resuscitation, and from male Sprague–Dawley rats at baseline and after 20 min CA followed by 30 min cardiopulmonary bypass resuscitation. An untargeted metabolomics evaluation using UPLC-QTOF-MS/MS was performed for plasma metabolome comparison. Here we show the metabolic commonality between humans and our severe injury rat model, highlighting significant metabolic dysfunction as seen by similar alterations in (1) TCA cycle metabolites, (2) tryptophan and kynurenic acid metabolites, and (3) acylcarnitine, fatty acid, and phospholipid metabolites. With substantial interspecies metabolic similarity in post-resuscitation plasma, our long duration CA rat model metabolically replicates human disease and is a suitable model for translational CA research.

Original languageEnglish
Article number19707
JournalScientific Reports
Volume10
Issue number1
DOIs
Publication statusPublished - Dec 2020
Externally publishedYes

Fingerprint

Dive into the research topics of 'Plasma metabolomics supports the use of long-duration cardiac arrest rodent model to study human disease by demonstrating similar metabolic alterations'. Together they form a unique fingerprint.

Cite this